Chapter 071. Vitamin and Trace Mineral Deficiency and Excess (Part 12)

ZincZinc is an integral component of many metalloenzymes in the body; it is involved in the synthesis and stabilization of proteins, DNA, and RNA and plays a structural role in ribosomes and membranes. Zinc is necessary for the binding of steroid hormone receptors and several other transcription factors to DNA. Zinc is absolutely required for normal spermatogenesis, fetal growth, and embryonic development.AbsorptionThe absorption of zinc from the diet is inhibited by dietary phytate, fiber, oxalate, iron, and copper, as well as by certain drugs including penicillamine, sodium valproate, and ethambutol. Meat, shellfish, nuts, and legumes are goodsources of bioavailable...
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Chapter 071. Vitamin and Trace Mineral Deficiency and Excess (Part 12) Chapter 071. Vitamin and Trace Mineral Deficiency and Excess (Part 12) Zinc Zinc is an integral component of many metalloenzymes in the body; it isinvolved in the synthesis and stabilization of proteins, DNA, and RNA and plays astructural role in ribosomes and membranes. Zinc is necessary for the binding ofsteroid hormone receptors and several other transcription factors to DNA. Zinc isabsolutely required for normal spermatogenesis, fetal growth, and embryonicdevelopment. Absorption The absorption of zinc from the diet is inhibited by dietary phytate, fiber,oxalate, iron, and copper, as well as by certain drugs including penicillamine,sodium valproate, and ethambutol. Meat, shellfish, nuts, and legumes are goodsources of bioavailable zinc, whereas zinc in grains and legumes is less availablefor absorption. Deficiency Mild zinc deficiency has been described in many diseases, includingdiabetes mellitus, HIV/AIDS, cirrhosis, alcoholism, inflammatory bowel disease,malabsorption syndromes, and sickle cell disease. In these diseases, mild chroniczinc deficiency can cause stunted growth in children, decreased taste sensation(hypogeusia), and impaired immune function. Severe chronic zinc deficiency hasbeen described as a cause of hypogonadism and dwarfism in several MiddleEastern countries. In these children, hypopigmented hair is also part of thesyndrome. Acrodermatitis enteropathica is a rare autosomal recessive disordercharacterized by abnormalities in zinc absorption. Clinical manifestations includediarrhea, alopecia, muscle wasting, depression, irritability, and a rash involvingthe extremities, face, and perineum. The rash is characterized by vesicular andpustular crusting with scaling and erythema. Occasional patients with Wilsonsdisease have developed zinc deficiency as a consequence of penicillamine therapy(Chap. 354). The diagnosis of zinc deficiency is usually made by a serum zinc level ofin hypozincemia. In acute stress situations, zinc may be redistributed from seruminto tissues. Zinc deficiency may be treated with 60 mg elemental zinc, orallytwice a day. Zinc gluconate lozenges (13 mg elemental zinc every 2 h whileawake) have been reported to reduce the duration and symptoms of the commoncold in adults, but studies are conflicting. Zinc deficiency is prevalent in many developing countries and usuallycoexists with other micronutrient deficiencies (especially iron). Zinc (20 mg/d)may be an effective adjunctive therapeutic strategy for diarrheal disease inchildren. Toxicity Acute zinc toxicity after oral ingestion causes nausea, vomiting, and fever.Zinc fumes from welding may also be toxic and cause fever, respiratory distress,excessive salivation, sweating, and headache. Chronic large doses of zinc maydepress immune function and cause hypochromic anemia as a result of copperdeficiency. Copper Copper is an integral part of numerous enzyme systems including amineoxidases, ferroxidase (ceruloplasmin), cytochrome-c oxidase, superoxidedismutase, and dopamine hydroxylase. Copper is also a component offerroprotein, a transport protein involved in the basolateral transfer of iron duringabsorption from the enterocyte. As such, copper plays a role in iron metabolism,melanin synthesis, energy production, neurotransmitter synthesis, and CNSfunction; the synthesis and cross-linking of elastin and collagen; and thescavenging of superoxide radicals. Dietary sources of copper include shellfish,liver, nuts, legumes, bran, and organ meats. Deficiency Dietary copper deficiency is relatively rare, although it has been describedin premature infants who are fed milk diets and in infants with malabsorption(Table 71-2). Copper-deficiency anemia has been reported in patients withmalabsorptive diseases and nephrotic syndrome and in patients treated forWilsons disease with chronic high doses of oral zinc, which can interfere withcopper absorption. Menkes kinky hair syndrome is an X-linked metabolicdisturbance of copper metabolism characterized by mental retardation,hypocupremia, and decreased circulating ceruloplasmin (Chap. 357). It is causedby mutations in the copper-transporting ATP7A gene. Children with this diseaseoften die within 5 years because of dissecting aneurysms or cardiac rupture.Aceruloplasminemia is a rare autosomal recessive disease characterized by tissueiron overload, mental deterioration, microcytic anemia, and low serum iron andcopper concentrations. The diagnosis of copper deficiency is usually made on the basis of lowserum levels of copper (